In human obesity, the stroma vascular fraction (SVF) of
white adipose tissue (WAT) is enriched in macrophages.
These cells may contribute to low-grade inflammation and
to its metabolic complications. Little is known about the
effect of weight loss on macrophages and genes involved in
macrophage attraction. We examined subcutaneous WAT
(scWAT) of 7 lean and 17 morbidly obese subjects before
and 3 months after bypass surgery. Immunomorphological
changes of the number of scWAT-infiltrating macrophages
were evaluated, along with concomitant changes in expression
of SVF-overexpressed genes. The number of sc-
WAT-infiltrating macrophages before surgery was higher
in obese than in lean subjects (HAM56+/CD68+; 22.6 +
4.3 vs. 1.4 + 0.6%, P < 0.001). Typical “crowns” of
macrophages were observed around adipocytes. Drastic
weight loss resulted in a significant decrease in macrophage
number (-11.63 + 2.3%, P < 0.001), and remaining
macrophages stained positive for the anti-inflammatory
protein interleukin 10. Genes involved in macrophage
attraction (monocyte chemotactic protein [MCP]-1, plasminogen
activator urokinase receptor [PLAUR], and colony-
stimulating factor [CSF]-3) and hypoxia (hypoxiainducible
factor-1a [HIF-1a]), expression of which
increases in obesity and decreases after surgery, were
predominantly expressed in the SVF. We show that improvement
of the inflammatory profile after weight loss is
related to a reduced number of macrophages in scWAT.
MCP-1, PLAUR, CSF-3, and HIF-1a may play roles in the
attraction of macrophages in scWAT.

In human obesity, the stroma vascular fraction (SVF) of
white adipose tissue (WAT) is enriched in macrophages.
These cells may contribute to low-grade inflammation and
to its metabolic complications. Little is known about the
effect of weight loss on macrophages and genes involved in
macrophage attraction. We examined subcutaneous WAT
(scWAT) of 7 lean and 17 morbidly obese subjects before
and 3 months after bypass surgery. Immunomorphological
changes of the number of scWAT-infiltrating macrophages
were evaluated, along with concomitant changes in expression
of SVF-overexpressed genes. The number of sc-
WAT-infiltrating macrophages before surgery was higher
in obese than in lean subjects (HAM56+/CD68+; 22.6 +
4.3 vs. 1.4 + 0.6%, P < 0.001). Typical “crowns” of
macrophages were observed around adipocytes. Drastic
weight loss resulted in a significant decrease in macrophage
number (-11.63 + 2.3%, P < 0.001), and remaining
macrophages stained positive for the anti-inflammatory
protein interleukin 10. Genes involved in macrophage
attraction (monocyte chemotactic protein [MCP]-1, plasminogen
activator urokinase receptor [PLAUR], and colony-
stimulating factor [CSF]-3) and hypoxia (hypoxiainducible
factor-1a [HIF-1a]), expression of which
increases in obesity and decreases after surgery, were
predominantly expressed in the SVF. We show that improvement
of the inflammatory profile after weight loss is
related to a reduced number of macrophages in scWAT.
MCP-1, PLAUR, CSF-3, and HIF-1a may play roles in the
attraction of macrophages in scWAT.